Dr. Bray Links

Saturday, December 1, 2018

A novel hypothesis for atherosclerosis as a cholesterol sulfate deficiency syndrome

Worldwide geographical data show an inverse relationship between cardiovascular disease and annual sunlight availability [18]. In a study conducted in the British Isles, 49 % of the variance in mortality from coronary heart disease was accounted for by mean annual sunshine hours as measured by the Meteorological Office [19]. However, placebo-controlled trials failed to show any benefit from vitamin D3 supplementation [20]. We propose that the benefit comes from Ch-S synthesis instead. In [16], it was proposed that the protein endothelial nitric oxide synthase (eNOS), along with sunlight, catalyzes sulfate production in erythrocytes, endothelial cells, platelets and keratinocytes in the skin. Thus, eNOS is a dual-purpose enzyme, producing sulfate when it is membrane–bound and producing nitric oxide when it is free in the cytoplasm. We hypothesize that the overuse of sunscreen has played a dual damaging role not only because sunlight catalysis is suppressed but also because the aluminum found in high-SPF sunscreens as an emulsifier actively disrupts eNOS' function [21]. eNOS is an orphan cytochrome P450 (CYP) enzyme [22], and aluminum is a known disruptor of CYP enzyme function through its displacement of the iron in the heme group [23]. Many other environmental toxicants also disrupt CYP enzymes, including mercury [24, 25], arsenic [26], cadmium [24], glyphosate [27, 28], and lead [25, 29].


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